ArticleNucleic acids research2001
Deletion of the CSB homolog, RAD26, yields Spt(-) strains with proficient transcription-coupled repair.
Article in Nucleic acids research, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 23 citations in OpenAlex.
- Proteome-wide signatures of function in highly diverged intrinsically disordered regions.eLife · 2019Article
- Molecular basis of chromatin remodeling by Rhp26, a yeast CSB ortholog.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Chromatin modifications and DNA repair: beyond double-strand breaks.Frontiers in genetics · 2014Review
- Rad26p, a transcription-coupled repair factor, promotes the eviction and prevents the reassociation of histone H2A-H2B dimer during transcriptional elongation in vivo.Biochemistry · 2012Article
- Rad26p regulates the occupancy of histone H2A-H2B dimer at the active genes in vivo.Nucleic acids research · 2012Article
- Modulation of Rad26- and Rpb9-mediated DNA repair by different promoter elements.The Journal of biological chemistry · 2006Article
- Cockayne syndrome group B cellular and biochemical functions.American journal of human genetics · 2003Review
- Rpb4 and Rpb9 mediate subpathways of transcription-coupled DNA repair in Saccharomyces cerevisiae.The EMBO journal · 2002Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
It has been previously shown that disruption of RAD26 in yeast strain W303-1B results in a strain that is deficient in transcription-coupled repair (TCR), the preferential repair of the transcribed strand of an expressed gene over the non-transcribed strand and the rest of the genome. RAD26 encodes a protein that is homologous to Cockayne syndrome group B protein (CSB) and is a member of the SWI2/SNF2 family of DNA-dependent ATPases involved in chromatin remodeling. Like the rad26 mutant, cells from Cockayne syndrome patients are defective in TCR. We examined the role of Rad26 in TCR by disrupting RAD26 in two repair-proficient laboratory strains and, remarkably, observed no effect upon TCR. Our results indicate that disruption of RAD26 alone is insufficient to impair TCR. Thus, W303-1B must already possess a mutation that, together with disruption of RAD26, causes a deficiency in TCR. We suggest that other genes are mutated in Cockayne syndrome cells that contribute to the deficiency in TCR. Surprisingly, deletion of RAD26 results in expression of genes that are repressed by flanking transposon delta elements, an Spt(-) phenotype. The delta elements appear to perturb local chromatin structure. Expression of genes flanked by delta elements in rad26Delta mutants is consistent with a role for Rad26 in chromatin remodeling.
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